Philip Teitelbaum

Sensory Neglect Produced by Lateral Hypothalamic Damage

Unilateral lateral hypothalamlic lesions in rats produce deficits in orientation to contralateral visucal, olfactory, whisker-toluch, and somatosetnsory stimuli. This syndrome of sensory neglect appears to be involved in some of the deficits in feedinig and attack which follow bilateral lateral hypothalamic lesions.

Hypothalamic Control of Feeding and Self-Stimulation

Hypothalamic sites which control feeding exert a corresponding control over lateral hypothalamic self-stimulation. This was demonstrated in rats bearing four, intrahypothalamic electrode-cannulas for electrical stimulation or chemical injection. Self-stimulation of the lateral hypothalamus was inhibited by ventromedial excitation or by excessive feeding. Both self-stimulation and feeding were accelerated (disinhibited) by ventromedial ablation or anesthetization. Thus food acts via the ventromedial hypothalamus to inhibit not only feeding, but also lateral hypothalamic self-stimulation.

Spreading Depression and Recovery from Lateral Hypothalamic Damage

Spreading cortical depression reinstates aphagia and adipsia in rats recovered from lateral hypothalamic lesions. We suggest that cortical activity facilitates and maintains recovery by enhancing the activity of depressed, but intact, tissue adjacent to the lesions.

STAGES OF RECOVERY AND DEVELOPMENT OF LATERAL HYPOTHALAMIC CONTROL OF FOOD AND WATER INTAKE

In 1951 Anand and Brobeck2 observed that destruction of a small area in the lateral hypothalamus in rats and cats led to loss of eating and death from starvation. In 1954 Teitelbaum and Stellarl6 found that rats with lateral hypothalamic damage not only starved but also refused to drink. However, if such rats were kept alive by tube-feeding and were offered a variety of wet and palatable foods in addition to the ordinary diet of dry Purina and water, they eventually recovered both feeding and drinking in a regular sequence. Such a gradual recovery of hypothalamic function through qualitatively discrete stages offers a remarkable opportunity for experimental fractionation of the multiple controls that ordinarily interact simultaneously to maintain normal intake. Even after the lateral hypothalamic animal eats and drinks again, thereby adjusting caloric intake and maintaining his body weight, recovery is not complete6JJ5 suggesting that some normal controls are permanently lost. In the first part of this paper, we will review our knowledge of the mechanisms of the lateral hypothalamic control of food and water intake, based on a detailed analysis of the pattern of deficits seen in various stages of recovery. Then, in the second part of the paper, we will present new findings which suggest that a parallel to adult recovery is seen in the pattern of infantile development of control of feeding and drinking.

Thermoregulatory cold-defense deficits in rats with preoptic/anterior hypothalamic lesions☆

This paper discusses the course of recovery from the thermoregulatory deficits produced in rats by electrolytic lesions in the preoptic/anterior hypothalamic area. Severe damage rendered rats ectothermic, that is unable to maintain their body temperatures at normal levels unless they were incubated at an ambient temperature of 30 degrees C. Less severe damage produced rats that maintained subnormal but stable body temperatures at 23 degrees C, but that did not increase metabolic rate or shiver and whose body temperatures dropped drastically in the cold (5 degrees C). As the animals recovered, nonshivering thermogenesis returned. Eventually the rats became excessively hyperthermic in normal room temperatures, due to very high metabolic rates. They were still unable to shiver or increase metabolic rate further in the cold and were therefore still unable to prevent a large drop in body temperature. Muscle tonus and shivering recovered gradually, and oxygen consumption returned to near normal levels. The data are described in terms of levels of integration of the nervous control of thermoregulation.

The contribution of oropharyngeal sensations to hypothalamic hyperphagia.

Abstract Hypothalamic hyperphagia was studied in rats that fed themselves food they could not taste or smell. Overeating persisted in the absence of oropharyngeal sensations. However, high levels of obesity were not reached. The addition of small oral incentives produced new bouts of overeating and rapid weight gain. Excessive responsiveness to highly palatable foods is not the cause of hypothalamic hyperphagia but oropharyngeal sensations determine the rate and duration of the overeating and are essential for maximum levels of obesity.